Vascular graft thrombosis secondary to activated protein C resistance: a case report and literature review

Abstract

Hypercoagulability is a well-documented and prominent risk factor for venous thromboembolism. The role of thrombophilia in arterial thrombotic events is less well defined. A 52-year-old male patient with multiple atherogenic risk factors was admitted for non-healing pedal ulcer and absent distal pulses. Based on the clinical presentation, Doppler ultrasound and angiography findings, the patient underwent elective in situ bypass arterial reconstruction. The saphenous vein graft was of satisfactory quality and the procedure went routinely. Acute graft thrombosis on postoperative day 0 was recognized immediately and prompted an emergent surgical revision. No technical errors or anatomical/mechanical causes for failed reconstruction were found and the graft was successfully thrombectomized using a Fogarty balloon-catheter. Graft rethrombosis, however, ensued after several hours. Considering the absence of threatening limb ischemia and the idiopathic recurrent thrombosis, raising suspicion of prothrombotic state, conservative treatment was pursued. Postoperative thrombophilia testing proved positive for activated protein C resistance, mandating introduction of chronic oral anticoagulation. Six months later, the operated extremity is viable. Inexplicable vascular graft thrombosis, particularly if early and recurrent, should raise suspicion of underlying thrombophilia. If confirmed by laboratory testing, long-term secondary antithrombotic prophylaxis may be required.

Concomitant Deep Venous Thrombosis, Femoral Artery Thrombosis, and Pulmonary Embolism after Air Travel

“…Due to the patient being lost to followup, we cannot investigate a possible hypercoagulable state which to this point has been unidentified. Case reports have attributed acute limb arterial thrombosis to a known hypercoagulable state (inherited [30] or acquired [31]) although the literature has not shown there be a statistical association between the two. In this case and similar cases, a hypercoagulable workup should include testing for Factor V Leiden and prothrombin 20210 mutations, deficiency of protein C, protein S, and antithrombin III; elevation of clotting factors VIII, IX, XI, and fibrinogen and homocysteine levels; and testing anticardiolipin antibodies.…”

Inflammatory skin diseases and wounds

“…Factor V Leiden mutation is a coagulation defect that can lead to postthrombotic venous leg ulcers and cutaneous necrosis, especially in homozygous affected individuals, due to an up to 100-fold increased tendency to thrombosis. 36 Disseminated intravascular coagulation (DIC) is a disorder with an abnormal coagulation state associated to infections, neoplasms, obstetric complications, vascular anomalies, trauma and other medical issues. 37 Cryoglobulinaemia and cryofibrinogenaemia are vasculopathies in which specific proteins precipitate when exposed to cold temperatures.…”

“…It appears that the treatment decreases protein C and protein S activity, promoting a hypercoagulable state, but there is also a potential toxic effect of coumadin on papillary dermal microvessels. Factor V Leiden mutation is a coagulation defect that can lead to post‐thrombotic venous leg ulcers and cutaneous necrosis, especially in homozygous affected individuals, due to an up to 100‐fold increased tendency to thrombosis 36 . Disseminated intravascular coagulation (DIC) is a disorder with an abnormal coagulation state associated to infections, neoplasms, obstetric complications, vascular anomalies, trauma and other medical issues 37 .…”